We report a case of leukocytoclastic vasculitis (LCV) in a 74-year-old woman, occurring seven months after the initiation of fluoxetine therapy for generalized anxiety disorder (GAD). The cutaneous lesions resolved upon discontinuation of fluoxetine but recurred promptly upon rechallenge. Notably, subsequent exposure to paroxetine, another selective serotonin reuptake inhibitor (SSRI) previously tolerated by the patient, also elicited a similar but less severe rash, suggesting cross-sensitization. Transition to venlafaxine, a serotonin-norepinephrine reuptake inhibitor (SNRI), led to complete and sustained resolution of the skin lesions. This case highlights three key clinical points: the potential for delayed-onset cutaneous adverse reactions to SSRIs even after months of uneventful treatment; the occurrence of cross-reactive hypersensitivity among SSRIs; and the importance of considering alternative antidepressant classes with distinct pharmacological profiles in patients with SSRI-associated vasculitis.

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare, potentially life-threatening immune-related adverse event that can be triggered by immune checkpoint inhibitors. We present the case of a 58-year-old woman with malignant acral melanoma who developed late-onset DRESS following sequential treatment with pembrolizumab and nivolumab. The patient initially developed a generalized erythrodermic, scaly rash with pruritus after the third dose of pembrolizumab, which recurred upon switching to nivolumab. Laboratory evaluation revealed leukocytosis, marked eosinophilia, transaminitis, and elevated lactate dehydrogenase. Skin biopsies demonstrated spongiosis, basal vacuolar degeneration, eosinophilic infiltrate, and leukocytoclastic vasculitis, consistent with DRESS. Despite corticosteroid therapy, the patient experienced multiple relapses triggered by immunosuppressant tapering, requiring prolonged cyclosporine treatment. Her presentation met the registry of severe cutaneous adverse reactions (RegiSCAR) criteria for definite DRESS. This case underscores the need for heightened awareness of delayed hypersensitivity reactions to immune checkpoint inhibitors and highlights the possibility of a chronic-relapsing course requiring extended immunosuppressive therapy.

Our manuscript presents a rare case of idiopathic mesenteric phlebosclerosis (IMP) in a 73-year-old woman who experienced recurrent abdominal pain and diarrhea. Through a detailed clinical investigation, including laboratory tests, colonoscopy, biopsy, and enhanced abdominal CTA, we diagnosed the patient with IMP. Notably, we identified a potential link between the patient's long-term intake of a traditional Chinese herb containing Gardenia Fructus and the development of IMP. This finding is supported by existing literature, which suggests that genipin, a component of Gardenia Fructus, may cause intimal hyperplasia and fibrosis of the venous wall, leading to chronic intestinal ischemia. Our case highlights the importance of considering herbal intake as a potential risk factor for IMP and underscores the need for clinicians to be aware of the potential adverse effects of traditional herbal remedies.

Angiotensin-converting enzyme (ACE) inhibitor-associated hypersensitivity vasculitis with gastrointestinal involvement is an uncommon but important drug-related cause of acute abdominal pain and may mimic an acute surgical abdomen. We report the case of an 84-year-old man admitted for redo aortic valve replacement following infective endocarditis, who developed acute abdominal pain on postoperative day 14. Physical examination revealed diffuse abdominal tenderness and cutaneous purpura. Laboratory testing showed elevated inflammatory markers with peripheral eosinophilia. Contrast-enhanced abdominal CT demonstrated concentric small bowel wall thickening with submucosal edema and ascites, without evidence of mesenteric ischemia. Skin biopsy confirmed leukocytoclastic vasculitis. Lisinopril was initiated at the time of admission and continued throughout the perioperative period; symptoms occurred approximately three weeks after treatment initiation, with no prior history of similar episodes. Discontinuation of lisinopril resulted in rapid clinical improvement and complete resolution of abdominal symptoms. This case highlights that ACE inhibitor-associated hypersensitivity vasculitis may present with small bowel edema and imaging findings overlapping with intestinal angioedema. Careful medication review and recognition of associated systemic features such as purpura and eosinophilia are essential to avoid unnecessary invasive procedures.

Cite this article as: Günegül Y, Tozlu M, Demiral YE, Eminler AT, Uslan Mİ. Leukocytoclastic vasculitis occurring during upadacitinib therapy in ulcerative colitis: A case report. Turk J Gastroenterol. 2026;37(4):529-531.

BACKGROUND Dalbavancin is a lipoglycopeptide antibiotic largely used to treat serious and complex bacterial infections, particularly those caused by gram-positive bacteria. Its main advantages include a prolonged half-life, which allows for once-weekly dosing, effectiveness against resistant pathogens, most notably, methicillin-resistant Staphylococcus aureus, and a good profile of tolerability and patient adherence. Herein we report the first documented case of a patient who developed palpable purpura on both lower limbs following treatment with dalbavancin, which was clinically and histologically diagnosed as leukocytoclastic vasculitis (LV). CASE REPORT A 66-year-old woman received dalbavancin due to an acute bacterial skin and skin structure infection (ABSSSI) of her right leg. The patient initially showed a favorable clinical response, with marked improvement of the infection. However, 3 weeks after the administration of dalbavancin, she developed a diffuse erythematous palpable purpura, predominantly affecting the lower limbs, and accompanied by mild arthralgia and generalized asthenia. To further investigate and confirm the underlying cause of these new symptoms, a skin biopsy was performed, revealing histopathological findings consistent with LV. Following the diagnosis, corticosteroid therapy was initiated, resulting in a significant symptomatic improvement. CONCLUSIONS To the best of our knowledge, this is the first published, histologically confirmed case report of LV developing after treatment with dalbavancin. Given the widespread use of dalbavancin for treating ABSSSIs, clinicians should be aware of the potential adverse effects, including LV, that may arise during its administration.

Vancomycin is a first-line antibiotic used for severe gram-positive infections, but it may rarely trigger immune-mediated small-vessel vasculitis. We report a case of a 43-year-old man with end-stage renal disease on home hemodialysis who developed palpable purpuric skin lesions three days after starting vancomycin for L5-S1 discitis and osteomyelitis. Over the following days, the eruption progressed into symmetric, non-blanching purpuric plaques involving the upper and lower extremities by day 6 of therapy. Laboratory evaluation demonstrated progressive thrombocytopenia, an increase in eosinophil counts within the normal reference range, and elevated inflammatory markers, which declined after vancomycin cessation. Vancomycin was discontinued, and antimicrobial therapy was transitioned to daptomycin, resulting in rapid clinical improvement within 48 hours and near-complete resolution by day 12. This case emphasizes the importance of early recognition of vancomycin-induced leukocytoclastic vasculitis, particularly in patients with renal impairment who may experience an accelerated onset. Prompt discontinuation of the offending agent typically results in rapid recovery without the need for systemic corticosteroids.

Digital necrosis is now a well-established complication of COVID-19 infection, but data are sparse regarding the pathophysiology. We present the case of digital necrosis secondary to cutaneous leukocytoclastic vasculitis in a patient with COVID-19 infection. After histologic confirmation of vasculitis, the patient was given methylprednisolone leading to an improvement that enabled limited amputation.

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that can rarely be complicated by systemic immune phenomena. We report a 41-year-old woman with severe HS refractory to adalimumab who developed fever, palpable purpura, and renal involvement. Skin biopsy confirmed IgA leukocytoclastic vasculitis, and renal biopsy revealed IgA nephritis. She was treated with corticosteroids, rituximab, and surgery, but proteinuria persisted. Initiation of bimekizumab led to marked improvement of HS lesions and a significant reduction in proteinuria. Over more than one year of follow-up, she achieved sustained HS control without recurrence of vasculitis or treatment-related adverse events. This case highlights the potential role of dual IL-17A/F inhibition in managing refractory HS complicated by IgA vasculitis and nephritis.

Coumarin derivatives, including warfarin and acenocoumarol, are widely used oral anticoagulants that inhibit vitamin K-dependent coagulation factors. They are commonly prescribed for the prophylaxis of thromboembolic disorders. Although effective, these agents are associated with many adverse drug reactions, which include hemorrhagic complications, warfarin-induced skin necrosis, hypersensitivity reactions, and, rarely, leukocytoclastic vasculitis (LCV). LCV is an immune-mediated small-vessel vasculitis characterised by palpable purpura, often triggered by drugs, infections, or autoimmune conditions. Here, we present the case of a 53-year-old female with a history of rheumatic heart disease and mechanical mitral valve replacement who developed LCV after 5 years on acenocoumarol. The reaction persisted despite adjunct therapy and worsened upon switching to warfarin, suggesting possible cross-reactivity between these coumarin derivatives. Ultimately, transitioning to apixaban led to the complete resolution of symptoms. This case underscores the importance of early recognition of drug-induced vasculitis and highlights the need for individualised anticoagulation strategies in patients with hypersensitivity reactions.